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Biomedical subjects

P Sipponen

Publications and source records attributed to P Sipponen.

At least 127 records · Page 7Linked to original sources
PubMed1992

Gastric changes in coronary-operated patients with low-dose aspirin.

Low-dose aspirin is widely used in patients operated on for coronary disease as secondary prevention of coronary artery occlusion. The changes caused by aspirin in therapeutic doses to gastric mucosa are well documented, but the effect of long-term low-dose aspirin is not so well known. Forty-six volunteer coronary-operated patients with daily low-dose aspirin were interviewed postoperatively, and an upper gastrointestinal tract endoscopy was performed and biopsy specimens taken 3 months after the operation. The findings were compared with a normal population sample of 358 persons from a study previously published. There were significantly more erosions and ulcers or fresh scars in the study group than in the control population--11 of 46 patients and 24 of 358 patients, respectively. The presence of superficial gastritis was similar. Mostly, the lesions were asymptomatic. History of peptic ulcer disease, use of other ulcerogenic drugs, smoking, and alcohol consumption had no predictive value for acute lesions. In contrast, the lesions were associated with chronic superficial gastritis and Helicobacter pylori infection.

Adult↗
PubMed1992

Gastric carcinoma: failed adaptation to Helicobacter pylori.

Helicobacter pylori is the major cause of chronic gastritis. Unlike bacterial infections in general, H. pylori acquisition causes a chronic, usually life-long infection. After acquisition, chronic inflammation (gastritis) appears and develops slowly into atrophic gastritis (with intestinal metaplasia) in a proportion of affected subjects. Inflammation and atrophy result from a failure of the immune system to eliminate the H. pylori infection. In infected stomach, several cascades of reactions are triggered which may result in impairments of structure and function of the gastric mucosa, some of which lesions also increase the risk of gastric carcinoma (CGA). A sequence of events from an early H. pylori infection into an atrophic gastritis has risen a theory that the H. pylori acquisition is a key issue in the development of GCA. Several aspects in the epidemiology and pathogenesis of GCA can be understood and explained by this infectious background. The H. pylori gastritis is unexpectedly common in patients with GCA of both intestinal or diffuse type, and the infection and gastritis precede the development of cancer. In Finland, 70-80% of the GCA cases seem to develop in connection with an H. pylori-positive gastritis or atrophy, 10-15% develop in a normal stomach (genetically determined GCA cases?), and 10-15% are associated with an H. pylori-negative corpus-limited (autoimmune) gastritis and atrophy. Case control studies suggest that the presence of H. pylori related inflammation raises the risk of GCA twofold, and the appearance of atrophic gastritis (and intestinal metaplasia) raises further this risk 2-3 times, as compared to the risk of GCA in subjects with a normal stomach.

Adaptation, Physiological↗
PubMed1991

Positive serum antibody and negative tissue staining for Helicobacter pylori in subjects with atrophic body gastritis.

Helicobacter pylori is rarely found in gastric biopsy specimens from individuals with atrophic gastritis of the body mucosa. To determine if subjects with atrophic body gastritis have evidence of previous infection with H. pylori, immunoglobulin G antibody to H. pylori was measured by enzyme-linked immunosorbent assay in sera of 399 Finnish subjects. In 124 subjects, multiple biopsy specimens from body and antrum had been evaluated for the presence of H. pylori by Giemsa staining. Antibody correlated well with H. pylori staining except in the subgroup with atrophic body gastritis, in whom the prevalence of seropositivity (86%) was significantly greater than the prevalence of positive staining (33%) (P less than 0.001). Twenty-five subjects had positive antibody and negative staining. This group had a significantly higher prevalence of atrophic body gastritis (80%), lower maximal acid output, lower serum pepsinogen I levels, and higher serum gastrin concentrations than did seropositive subjects with H. pylori. These data suggest that most patients with atrophic body gastritis, despite having a low incidence of current overt infection, have been infected with H. pylori at some point in their lives.

Adult↗
PubMed1991

Gastric cancer associated structure in mucus glycoproteins shown as a clinically useful marker.

A new monoclonal antibody has been developed which is capable of detecting structures in gastric mucus glycoproteins expressed in the fetus and in adult gastric mucosa in conditions such as gastric carcinoma. Cancer associated monoclonal antibodies were selected by testing them against various mucous glycoprotein samples from the alimentary tract, including salivary glycoproteins from both secretory and non-secretory subjects, and cancerous and normal gastric juice glycoproteins. They were tested against 1000 samples of gastric juice from an unselected population. Immunochemical characterisation suggested that the glycoproteins picked up by P4 and i11 include one of the compounds reacting with rabbit anti-fetal sulphoglycoprotein antigen serum. On the basis of a clinical trial and immunohistological evaluation further evidence was obtained of P4 as the most promising antibody for further experimentation. A total of 302 gastric juice specimens from patients with various gastric symptoms were analysed using the enzyme linked immunosorbent assay technique and P4 antibody. Of 10 gastric cancers, nine had P4 in the gastric juice. A positive correlation was found between gastric ulcer and the appearance of P4. Duodenal ulcers were not correlated to P4. Atrophic gastritis and P4 coincided less frequently. Raised P4 values were found in between 3% and 9% of subjects, depending on the population. Cancer cases showed high P4 values, which allows adjustment of the lower limit of a positive result to high level whereby a considerable number of non-cancerous P4 positives are omitted.

Antibodies, Monoclonal↗
PubMed1991

Dysplasia and carcinoma in longstanding ulcerative colitis: an endoscopic and histological surveillance programme.

From 1976 to 1989 a total of 66 patients with longstanding ulcerative colitis were entered in a colonoscopic surveillance programme in order to detect dysplasia. Thirty patients had extensive or total ulcerative colitis and 36 left sided colitis. The median duration of the disease at the end of the follow up was 15.0 years. Altogether 182 colonoscopies (2.8 per patient), each involving approximately 20 biopsies from different sites of the colon, were performed. In the total or extensive colitis group, five patients had low grade and one patient had high grade dysplasia. In the left sided colitis group, three patients had low grade dysplasia. In three patients low grade dysplasia was detected in a macroscopic lesion or mass of colonic mucosa. Sixty per cent of the dysplasia specimens were from the right colon. The incidence of dysplasia was higher in patients with extensive colitis and increased with the duration of the disease. None of the patients have so far developed colorectal carcinoma. Our results indicate that a colonoscopic surveillance programme is a safe alternative to prophylactic colectomy in longstanding ulcerative colitis.

Adolescent↗
PubMed1991

Disappearance of gastritis after eradication of Helicobacter pylori. A morphometric study.

Helicobacter pylori infection is strongly associated with and is considered a common cause of gastritis. To study the relationship between H. pylori and gastritis, we examined whether a reduction occurs in acute granulocytic and chronic mononuclear inflammation of gastric mucosa after eradication therapy. The examination is based on morphometric counting and on semiquantitative estimation of the density of the inflammatory cells in endoscopic biopsy specimens from antrum and corpus. The series consisted of 23 consecutive outpatients with H. pylori-associated gastritis who received a 2-week course of triple therapy with colloidal bismuth subcitrate, amoxicillin, and metronidazole and who underwent an endoscopic follow-up for 6 weeks, 6 months (23 patients), and 12 months (21 patients). The eradication was successful in 20 patients ('responders'), who also remained H. pylori-free for 6 months, and in 18 examined patients for 12 months but was unsuccessful in 3 patients ('non-responders'). Both acute and chronic inflammation decreased significantly in intensity in responders in the follow-up. The acute inflammation had already disappeared at a 6-week control. The reduction in chronic inflammation was slower and occurred gradually within the study. At the 12-month follow-up, the corpus mucosa was interpreted as normal in all 18 patients studied, and the antral mucosa was interpreted as normal in 10 (56%) patients. No significant reduction in intensity of gastritis was found in the 3 non-responders or the 23 matched, untreated controls. We conclude that the eradication of H. pylori results in a disappearance of both acute and chronic gastritis. This supports the view that H. pylori plays a causal role in the pathogenesis of chronic gastritis.

Acute Disease↗
PubMed1991

Characteristics of gastric mucosa which precede occurrence of gastric malignancy: results of long-term follow-up of three family samples.

The aim of the study was to evaluate what family characteristics and what morphological, functional and immunological changes of the gastric mucosa precede the development of gastric malignancy in a follow-up of 11-14 years. The material consisted of 301 first-degree relatives of gastric carcinoma patients, 183 relatives of pernicious anaemia patients, and of 358 control relatives of probands computer matched from the general population by age and sex for the carcinoma probands. All subjects were endoscopically examined in 1973-1976 and followed up to the end of 1987. According to cancer registry data, 11 cases of malignant gastric tumours (9 carcinomas, one carcinoid tumour and one anaplastic tumour with suspicion of Hodgkin's disease) had been diagnosed during the follow-up: 6 belonged to gastric carcinoma, 2 to pernicious anaemia and 3 to control families. The occurrence of malignancy was significantly related to the presence of advanced gastritis with atrophy and of intestinal metaplasia before the start of the follow-up. In relatives with achlorhydria and low serum pepsinogen I levels the incidence of malignancy did not significantly differ from that in controls of similar age and sex distribution. The risk of getting malignancy was about four-fold in female members of gastric carcinoma and pernicious anaemia families but was not increased in control families. The risk was increased only in female members and concerned only gastric malignancy being the expected one or even lower than the expected in regard to malignancies of other location.

Anemia, Pernicious↗
PubMed1991

Young onset peptic ulcer disease and non-ulcer dyspepsia are separate entities.

The characteristics of peptic ulcer and non-ulcer dyspepsia in young men were studied in 202 consecutive conscripts who attended Central Military Hospital in Helsinki because of long-standing upper abdominal complaints. Active peptic ulceration (APU) was found in 48 patients, inactive peptic ulcer disease (IPU) was diagnosed in 77 patients, non-ulcer dyspepsia (NUD) was diagnosed in 52 patients. In 25 cases the reason for symptoms was another disease, and these patients were excluded from the study. A control series (CON) consisted of 30 symptomless healthy young male volunteers. The likelihood of discriminating between peptic ulcer disease and non-ulcer dyspepsia in a young male patient with dyspepsia are indicated by odds ratios (OR) and its 95% confidence limits (CL 95). Active peptic ulcer disease differs from NUD, e.g., by 1) presence of antrum gastritis, OR 41.5 (CL 95: 10.1-171), 2) Helicobacter pylori in the gastric mucosa, OR 31.0 (7.4-130), 3) Lewisa+ phenotype, OR 8.9 (1.7-45.4), 4) serum pepsinogen I (S-PGI) greater than 100 micrograms/l, OR 4.6 (1.7-12.4), 5) non-secretor status, OR 4.3 (1.6-11.6), and 6) O-blood group, OR 3.0 (1.2-7.7). In conclusion, the status of gastroduodenal mucosa, gastric secretion pattern and distribution of some genetic markers in patient series indicate that young onset peptic ulcer and non-ulcer dyspepsia are two separate entities. Helicobacter-positive antrum gastritis is the best determinant of ulcer risk, but also high S-PGI, Lewisa+ phenotype, non-secretor status and O-blood group are signs of increased risk of peptic ulcer.

Adolescent↗
PubMed1991

Helicobacter pylori and duodenal ulcer. A study of duodenal ulcer patients and their first-degree relatives.

Out of 59 duodenal ulcer (DU) probands and their 199 first-degree relatives Giemsa-staining for the determination of Helicobacter pylori (HP) was performed in 51 probands and 155 relatives. Controls were matched by age and sex from a family sample representing the same geographical area. In all, 155 controls were found for the probands and relatives. The occurrence and score of HP density showed an excellent correlation with morphology of the mucosa, signs of acute inflammation and presence of gastric metaplasia in the duodenal bulb. The prevalence of HP was 94% in DU probands and significantly higher than in their relatives and controls. In sibs of DU probands the prevalence of HP (64%) was also significantly higher than in controls (51%) obviously due to the presence of a subgroup of sibs with signs of active or past duodenal ulcer disease, which show higher than expected prevalence of HP, and of acid hypersecretion and high levels of serum pepsinogen I (PG I). Peak acid output (PAO), serum pepsinogen I and II and fasting serum gastrin levels were in relatives without atrophy higher in HP positive than negative cases but significant differences were present only with regard to the pepsinogens. The occurrence of HP positivity as well as of high PAO and pepsinogen levels might be considered risk factors of DU disease in close relatives of DU probands. On the other hand, the significance of HP positivity as cause of abdominal complaints is doubtful, in view of the complete lack of correlation between HP and morphology and complaints in the present study.

Adult↗
PubMed1991

Functional characteristics of duodenal ulcer patients and their first-degree relatives.

The behaviour of acid secretion, serum pepsinogen I and II (PG I and PG II) and morphology of the gastric mucosa were analyzed in 59 duodenal ulcer probands (DU probands), their 199 first-degree relatives and 228 control subjects. DU probands had as a rule antral gastritis with normal or slightly altered corpus mucosa, and higher mean peak acid output (PAO), PG I and II levels than their relatives and controls. Sibs of DU probands differed from their controls mainly with regard to morphology which showed features characteristic of DU probands, i.e. antral gastritis with normal or slightly altered corpus mucosa. Moreover, high PAO levels were found highly significantly more often in sibs of DU probands (13%) than in controls (6%). Likewise, the prevalence of endoscopic signs of active or past duodenal ulcer were present in sibs highly significantly more often than in controls and they accumulated in the subgroup of sibs with high PAO or PG I levels. It seems probable that the occurrence of high PAO and PG I levels in sibs of DU probands can be considered as signs of increased liability to duodenal ulcer. PAO and PG I were as expected significantly higher in male than in female probands, relatives and controls. Exclusion of cases of corpus gastritis decreased the levels but the sex difference persisted. PAO, PG I and II revealed a significant increase of the levels in middle age followed in older age in case of PAO and PG I by a significant decrease. The decrease was abolished when the cases of corpus gastritis were excluded suggesting an effect of gastritis. However, the earlier increase of the levels remained virtually unaffected although there was a uniform decrease of the mean values. This suggests the participation of factors unrelated to gastritis. The nature of the factors remains unknown, but literature data and data derived from our recent study suggest involvement of anatomical factors such as an increase in the size of acid and PG I secreting area.

Adolescent↗
PubMed1991

Increase of serum pepsinogen I with age in females with normal gastric mucosa but not in males, possibly due to increase in acid-pepsin secreting area.

The mean pepsinogen I (PG I) level in a Finnish family sample was different in males and females and the difference was statistically significant. After exclusion of subjects with gastritis there remained 67 females and 68 males with morphologically completely normal antral and corpus mucosa. In females there was a significant increase of PG I with advancing age, the regression coefficient being 0.37 and statistically significant (p less than 0.01). In males no such increase was found, and individual cases revealed an almost random distribution with age. A similar increase with age has been noted in gastric acid output in females but not in males. Assuming that there is a linear relationship between PG I levels and the total chief cell mass, the PG I level would be determined by three main variables: thickness of the glandular layer, density of chief cells, and area occupied by chief cells. Of these variables the thickness and chief cell density showed neither in females nor in males any statistically significant increase with age, leaving the area as the variable which would account for the increase of PG I.

Adult↗
PubMed1991

Grade of Helicobacter pylori colonisation, chronic gastritis and relative risks of contracting high gastric ulcers: a seven-year follow-up.

A series of 38 patients with high gastric ulcer (GU) was examined twice a seven-year interval. One-third of the patients had an active ulcer at the second examination. Chronic gastritis was evaluated, and the level of Helicobacter pylori (HP) colonisation assessed semiquantitatively. The results were compared with age and sex matched non-ulcer controls. The GU series differed from the controls in having a higher degree of HP colonisation in gastric mucosa. The relative risks (RR) in predicting high GU connected with high HP colonisation were significantly elevated, both in the antrum (RR = 6.0-4.8) and in the corpus (RR 5.0-4.4), and still higher when combined HP colonisation values were used (RR 9.5-7.1). The persistence of active ulcer (GU+) was associated with a very high level of HP colonisation, with absence of corpus atrophic gastritis at the first examination and with young patients. Half of the GU+ patients had the maximum grade of combined HP colonisation in both examinations. The study indicates that the presence of HP infection as well as the level of HP colonisation are of importance in both the development and chronicity of peptic GU disease.

Adult↗
PubMed1991

What fraction of hospital ulcer patients is eligible for prospective drug trials?

Data of all 397 gastric ulcer patients diagnosed and treated at Jorvi Hospital, Finland, during 1980-1984 were collected and the outcome followed up for 5-7 years. The commonly used exclusion criteria of prospective drug trials were applied to this series. Only 29% of patients would have been eligible for a trial. The excluded patients were older, their ulcer was larger and more proximally located. Nearly all major complications of gastric ulcer disease leading to surgery (bleeding, perforation, obstruction) and deaths due to gastric ulcer disease appeared in the excluded group. Exclusion criteria may profoundly affect the selection of patients and the results. When many patients are excluded the applicability of results to the whole material is questionable.

Clinical Trials as Topic↗
PubMed1991

Helicobacter pylori: histological and serological study on gastric and duodenal ulcer patients in Estonia.

We have examined the occurrence of Helicobacter pylori (HP) infection in 86 Estonian gastric ulcer (GU) and 25 duodenal ulcer (DU) patients. Diagnosis of the HP infection was made histologically (modified Giemsa) from gastric biopsy specimens, and serologically by parallel use of two enzyme-linked immunosorbent assays for IgG antibodies to HP in patient sera. The infection was diagnosed simultaneously by all three methods in 84% of the GU and 84% of the DU patients. The infection was revealed histologically in 88% of the GU and 92% of the DU patients, and serologically by either of the two methods in 94% and 92% of the GU and DU patients, respectively. HP infection was absent by all three methods in one GU patient only, this patient being the only subject who showed normal gastric mucosa in conventional histology. These observations show that HP infection is very common in patients with peptic ulcer in Estonia. In addition, the findings suggest that the serological assays will find a small proportion (15%) of ulcer patients with antibodies against HP but no histologically detectable bacteria.

Adult↗
PubMed1991

Argyrophil cell hyperplasia associated with chronic corpus gastritis in gastric ulcer disease.

Argyrophil cell (AC) hyperplasia in corpus mucosa was investigated in 53 patients with chronic gastric ulcer disease not previously treated with antisecretory drugs. Mucosal biopsies were taken stepwise from the posterior wall in the corpus area of the stomach. Of 117 biopsy sites, 28 showed gastritis without atrophy, 85 showed chronic atrophic gastritis of varying degrees while 4 biopsies showed a normal mucosa. About one third (38%) showed a normal AC pattern. Of the remaining two thirds (62%), 45% had simple AC hyperplasia, 18% had linear and 37% had micronodular AC hyperplasia. A strong association was found between focal (linear/micronodular) AC hyperplasia and chronic atrophic gastritis. It is concluded that focal AC hyperplasia is a common phenomenon in gastric ulcer patients and is inherently related to the spontaneous development of atrophy in the corpus mucosa of these patients.

Adult↗
PubMed1991

Serum pepsinogen I and serum gastrin in the screening of atrophic pangastritis with high risk of gastric cancer.

Serum pepsinogen I (S-PGI) and serum gastrin (S-gastrin) were examined in the screening of three types of atrophic gastritis with inherent high risk of gastric cancer: in 102 cases with severe atrophic corpus gastritis (SACG), in 5 cases with severe atrophic antrum gastritis (SAAG), and in 15 cases with severe atrophic pangastritis (SAPG) (atrophy both in corpus and in antrum) found among 916 subjects from three family series (265 from gastric cancer families, 425 from randomly selected control families and 226 from pernicious anaemia families). There is no way to screen directly atrophic gastritis restricted to the antral mucosa. In pangastritis atrophy of antral glands causes a failure of the hypergastrinemic reaction of achlorhydria. The combination of S-PGI less than 25 micrograms/l + S-gastrin less than 200 pmol/l detected 80.0% of our cases with SAPG, and only 17 subjects of 794 (2.1%) were false positives i.e. who had not advanced atrophic gastritis. The risk of gastric cancer may be significantly higher in SAPG than in SACG. The estimated prevalence of SAPG was 3% in random-family members over 60 years. The combination of S-PGI and S-gastrin is recommended when the cost/benefit ratio in the screening program of gastric cancer is considered and people from a general population are selected for endoscopic studies.

Anemia, Pernicious↗
PubMed1991

Chronic gastritis: progression of inflammation and atrophy in a six-year endoscopic follow-up of a random sample of 142 Estonian urban subjects.

To study the prevalence and course of chronic gastritis (CG), 142 adult subjects collected at random from an Estonian urban area were endoscopically and bioptically examined at a six-year interval. The histology of the antral and corpus mucosae was evaluated by grading gastritis without ("superficial gastritis"; SG) and with atrophy ("atrophic gastritis"; AG) into mild, moderate and severe categories. A total of 135 (95%) and 139 (98%) subjects showed CG in the 1st and 2nd examinations, respectively. The CG healed in one subjects (0.7%), and in 5 out of 7 subjects with normal stomach in the 1st examination the CG started during the follow-up. No change in the severity of CG was seen in 24% of subjects with gastritis in the 1st examination. The main trend of CG was a slow, "one-step progression" in severity of inflammation and appearance of atrophy and intestinal metaplasia. Inflammation progressed significantly, especially in the young age groups and in the antrum in particular. The prevalence of AG increased linearly with age in corpus (mean annual risk 1.25%). Parietal cell antibodies (PCA) were found in 2 subjects in the 1st examination, and a further 2 subjects developed these antibodies later. Three of four PCA-positive subjects belonged to a subgroup of 8 elderly subjects who had corpus AG at both examinations and who also showed normal or normalizing mucosa in the antrum. It is concluded that CG is a slowly progressive disease advancing with time and, once started, rarely healing spontaneously.

Adolescent↗